Role of noroviruses as aetiological agents of diarrhoea in developing countries

Ayukekbong, James A; Mesumbe, Henry Nzike; Oyero, Olufunmilayo G; Lindh, Magnus; Bergström, Tomas

doi:10.1099/vir.0.000194

Cited by 24 publications

(25 citation statements)

References 195 publications

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“…These findings also indicate that asymptomatic infections could be a source of NoV outbreaks. Similarly, Ayukekbong et al [34] reported that in developing countries NoV infections are very common with comparable detection rates observed in diarrhea cases and controls. However in a cross-sectional study, it is easy to mis-classify substantial numbers of post-symptomatic infections as asymptomatic infections even when the controls are defined as absence of diarrhea symptoms in the preceding 4 weeks [35], [36], [37].…”

Section: Discussionmentioning

confidence: 71%

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Kabue

Meader

Hunter

et al. 2016

Journal of Clinical Virology

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Section: Discussionmentioning

confidence: 71%

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Kabue

Meader

Hunter

et al. 2016

Journal of Clinical Virology

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“…Data from Western countries and Japan have demonstrated that NoVs are responsible for 5%-30% of NoV asymptomatic infection in adults (Centers for Disease Control and Prevention, 2011;Ozawa et al, 2007), and that asymptomatic persons can spread the virus although their viral titer is usually lower than those of symptomatic persons. Moreover, NoV infections sometimes result in subclinical symptoms, which makes clinical diagnoses difficult (Ayukekbong et al, 2015). Asymptomatic NoV infection seems to contribute more to the spread of NoV infection in developing countries than in developed countries, because the number of people living in a household in developing countries is usually higher and the environmental sanitation level in these regions is often not optimal.…”

Section: Introductionmentioning

confidence: 99%

Occurrence of norovirus infection in an asymptomatic population in Indonesia

Utsumi

Lusida

Dinana

et al. 2017

Infection, Genetics and Evolution

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Norovirus (NoV) is a major cause of nonbacterial acute gastroenteritis worldwide in all age groups, and asymptomatic individuals may contribute to NoV transmission as a reservoir. Nonetheless, little information is available regarding asymptomatic NoV infection in Indonesia. We performed an epidemiological analysis of NoV infection among asymptomatic healthy volunteers in the city of Surabaya, Indonesia (population ~2.75 million). A total of 512 stool samples from 18 individuals (age range 20-42years) collected from July 2015 to June 2016 were examined. The detection of NoV and the genotype classification were carried out by a reverse transcription-polymerase chain reaction (RT-PCR) direct sequencing method. NoV was detected in 14 of the 512 stool samples (2.7%), with 7 individuals (38.9%) having at least 1 positive stool sample. All 14 of the NoV strains detected belonged to genogroup GII. The phylogenetic analysis indicated that 10 strains (71.4%) were grouped with GII.2, 2 (14.3%) were GII.17, 1 was GII.4 Sydney 2012, and 1 was GII.1. The circulation of GII.Pg/GII.1 and GII.Pe/GII.4 Sydney 2012 recombinant variants was detected among an asymptomatic population in Surabaya, Indonesia. Of the 7 positive individuals, 2 were repeatedly infected with the same strain and heterogenous strains. Taken together, our results suggest that the excretion of NoV from healthy individuals is one of the sources of NoV outbreak.

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“…Viruses within the genera Norovirus and Sapovirus in the family Caliciviridae are significant causes of gastroenteritis in humans and animals, with noroviruses alone causing ∼200,000 deaths per annum in children <5 years of age (2, 3). Despite their socioeconomic impact, the fastidious nature of viruses within these genera has significantly hindered our understanding of their life cycles and the development of vaccines and therapeutics (4, 5).…”

Section: Introductionmentioning

confidence: 99%

Activation of COX-2/PGE ₂ Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production

Alfajaro

Choi

Kim

et al. 2017

J Virol

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Enteric caliciviruses in the genera Norovirus and Sapovirus are important pathogens that cause severe acute gastroenteritis in both humans and animals. Cyclooxygenases (COXs) and their final product, prostaglandin E2 (PGE2), are known to play important roles in the modulation of both the host response to infection and the replicative cycles of several viruses. However, the precise mechanism(s) by which the COX/PGE2 pathway regulates sapovirus replication remains largely unknown. In this study, infection with porcine sapovirus (PSaV) strain Cowden, the only cultivable virus within the genus Sapovirus, markedly increased COX-2 mRNA and protein levels at 24 and 36 h postinfection (hpi), with only a transient increase in COX-1 levels seen at 24 hpi. The treatment of cells with pharmacological inhibitors, such as nonsteroidal anti-inflammatory drugs or small interfering RNAs (siRNAs) against COX-1 and COX-2, significantly reduced PGE2 production, as well as PSaV replication. Expression of the viral proteins VPg and ProPol was associated with activation of the COX/PGE2 pathway. We observed that pharmacological inhibition of COX-2 dramatically increased NO production, causing a reduction in PSaV replication that could be restored by inhibition of nitric oxide synthase via the inhibitor N-nitro-l-methyl-arginine ester. This study identified a pivotal role for the COX/PGE2 pathway in the regulation of NO production during the sapovirus life cycle, providing new insights into the life cycle of this poorly characterized family of viruses. Our findings also reveal potential new targets for treatment of sapovirus infection.IMPORTANCE Sapoviruses are among the major etiological agents of acute gastroenteritis in both humans and animals, but little is known about sapovirus host factor requirements. Here, using only cultivable porcine sapovirus (PSaV) strain Cowden, we demonstrate that PSaV induced the vitalization of the cyclooxygenase (COX) and prostaglandin E2 (PGE2) pathway. Targeting of COX-1/2 using nonsteroidal anti-inflammatory drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and the COX-2-specific inhibitors NS-398 and celecoxib or siRNAs targeting COXs, inhibited PSaV replication. Expression of the viral proteins VPg and ProPol was associated with activation of the COX/PGE2 pathway. We further demonstrate that the production of PGE2 provides a protective effect against the antiviral effector mechanism of nitric oxide. Our findings uncover a new mechanism by which PSaV manipulates the host cell to provide an environment suitable for efficient viral growth, which in turn can be a new target for treatment of sapovirus infection.

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Role of noroviruses as aetiological agents of diarrhoea in developing countries

Cited by 24 publications

References 195 publications

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Occurrence of norovirus infection in an asymptomatic population in Indonesia

Activation of COX-2/PGE ₂ Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production

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Role of noroviruses as aetiological agents of diarrhoea in developing countries

Cited by 24 publications

References 195 publications

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Norovirus prevalence and estimated viral load in symptomatic and asymptomatic children from rural communities of Vhembe district, South Africa

Occurrence of norovirus infection in an asymptomatic population in Indonesia

Activation of COX-2/PGE 2 Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production

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Activation of COX-2/PGE ₂ Promotes Sapovirus Replication via the Inhibition of Nitric Oxide Production